Recently, a newly described gastrointestinal hormone, pancreatic polypeptide (PP), has been found to be directly or indirectly related to appetite and weight control. It has been hypothesized that variations from normal in the secretion of this hormone might be a predictor of increased risk for obesity or possibly be directly involved in the pathogenesis of obesity through an effect on appetite. We have recently found that children with obesity and hyperphagia associated with the Prader-Willi syndrome (P-W,S) do not secrete PP in response to a standard meal as 23 control patients did. Our observations are not sufficient in themselves to implicate PP as a primary regulator of satiety, nor implicate this hormone (or the absence of this hormone) in the pathogenesis of this disorder. However, the absence of PP release in this human model of hyperphagia parallels previous observations in animal models of obesity and hyperphagia, is consistent with other observations showing blunted PP release in obese but healthy adults and suggests that PP may have a direct role in appetite control or may be directly affected by another putative satiety agent. This study is designed to: 1) explore the refractoriness of PP release in children with P-W,S 2) determine the PP response patterns in obese but otherwise normal children and compare these responses to those obtained in normal children. 3) investigate PP release in patients identified as having other clinical forms of altered appetite and weight, such as adolescents with anorexia nervosa and bulimia (recurrent episodes of binge eating). Pancreatic polypeptide secretion will be correlated with the patient's nutritional state, FFA levels and to other hormonal responses (insulin, gastric inhibitory peptide and cholecystokinin) which have been shown to be altered in adults with obesity or to be important in appetite control. 4) Finally, infusion of PP will be give to our children with P-W,S to test directly for it's satiety suppressent effects.